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Breast Cancer Treatment Linked to a Reduction in Alzheimer’s Disease Risk

Photo by National Cancer Institute on Unsplash

A Korean population-based cohort study investigated the risk of Alzheimer’s disease (AD) among breast cancer survivors compared to age-matched controls without cancer. The study, published in JAMA Network Open, found that breast cancer survivors had an 8% lower risk of AD than controls, with a significant association in survivors over 65 years old – though the effect did not persist past five years. Radiotherapy was associated with a lower risk of AD among breast cancer survivors – but not other treatments.

Breast cancer survivors may experience long-term health consequences, including cognitive function and risk of dementia. The risk of AD among breast cancer survivors is still unclear and may vary depending on age at diagnosis, treatment received, and time since treatment.

Previous studies reported mixed results on the risk of AD among breast cancer survivors, with some finding no increase in risk and others finding a 35% increased risk for those diagnosed at age 65 or older. These studies have been hampered by a number of methodological issues, including not accounting for risk factors.

Cytotoxic chemotherapy can cause cognitive decline termed ‘chemobrain’. Other chemotherapy drugs such as anthracycline may reduced AD risk by reducing the formation of amyloid deposits. Endocrine therapy may increase the risk of dementia by lowering oestrogen, but studies suggest that the use of tamoxifen and aromatase inhibitors is associated with a lower risk of AD. An increase in dementia is seen in radiotherapy for head and neck cancers.

To investigate the risk of AD among breast cancer survivors, researchers used the Korean National Health Insurance Service (K-NHIS) database, exploring whether there is an association with cancer treatment and various confounding factors.

Among 70 701 breast cancer survivors (mean age, 53.1 years), 1229 cases of AD were detected, with an incidence rate of 2.45 per 1000 person-years. Survivors exhibited a slightly lower risk of AD compared with cancer-free controls, especially among individuals 65 years or older (SHR, 0.92; 95% CI, 0.85-0.99). But landmark analyses found that this lower risk did not persist beyond five years of survival. Radiotherapy was associated with reduced risk of AD among survivors, while chemotherapy and endocrine therapy had no significant impact. Anthracycline use, however, did show a non-significant decrease in risk.

Differences in doses and timing of radiotherapy may influence the effects. The incident exposure to the brain is estimated to be 0.2Gy from a breast cancer radiotherapy dose of 50Gy. A pilot study found that patients with AD who received low-dose whole-brain radiotherapy at 3Gy showed a temporary improvement in cognitive function. This improvement is believed to be due to a neuroprotective effect on microglia. Other studies have noted a transient risk reduction for AD in breast cancer radiotherapy; however, patients receiving radiotherapy usually do so in conjunction with breast-conserving surgery – those opting for this procedure are younger, with fewer comorbidities and smaller tumours.

The study suggests that cancer treatment may have benefits against AD development, but the risk of AD may differ depending on the duration of survival.

The findings indicate that breast cancer treatment may not directly lead to AD, and that managing modifiable risk factors for AD, such as smoking and diabetes, is a feasible option to lower AD risk among breast cancer survivors.

Amid Surge in Cases, UK’s NHS to Offer Gonorrhoea Vaccine


Neisseria gonorrhoeae Bacteria Scanning electron micrograph of Neisseria gonorrhoeae bacteria, which causes gonorrhoea. Captured by the Research Technologies Branch (RTB) at the NIAID Rocky Mountain Laboratories (RML) in Hamilton, Montana. Credit: NIAID. Photo by National Institute of Allergy and Infectious Diseases on Unsplash

In the midst of a record high in gonorrhoea cases, the NHS is to offer a gonorrhoea vaccine to gay and bisexual men with a history of multiple partners or a sexually transmitted infection (STI), the BBC reports. The gonorrhoea vaccination, which is actually a repurposed meningococcal vaccine, is estimated only to be 30–40% effective. Research shows, however, that this will be sufficient to reduce cases and their attendant costs to the NHS.

Gonorrhoea is caused by the bacterium Neisseria gonorrhoeae and is typically transmitted by having intercourse without a condom. It can cause pain, unusual discharge, genital inflammation and infertility. Evidence has shown that the MeNZB and four-component serogroup B meningococcal (4CMenB) vaccines, designed against Neisseria meningitidis, can also offer protection against gonorrhoea.

In 2023, there were more than 85 000 cases – the highest since records began in 1918. A study published in The Lancet estimates that gonorrhoea vaccination would prevent 100 000 cases, saving the NHS £7.9 million over the next decade.

While gonorrhoea is treatable with antibiotics, resistance is growing and there is concern that it may eventually become untreatable. According to The Guardian, some cases are now “extensively drug resistant” (XDR) – not responsive to ceftriaxone or the second line of treatment. There were 17 cases of ceftriaxone-resistant gonorrhoea between January 2024 and March 2025, the UK Health Security Agency (UKHSA) reported.

Over the same period, nine XDR cases were reported, while between 2022 and 2023, there were only five.

The people most affected by gonorrhoea in the UK are the 16 to 25 age group, gay and bisexual men, and those of black and Caribbean ancestry. The study’s scenario for vaccinating at-risk populations included those who had more than five sexual partners per year or who had a positive gonorrhoea test.

The vaccine, costing about £8 per dose, is cost-effective when administered to this at-risk group of men, rather than adolescents. Despite this, clinicians will be able to offer the vaccine to anyone who, in their judgment, would benefit from it. Other vaccines such as for mpox – another STI with high transmission between gay and bisexual men – and hepatitis will also be offered.

Court Rules that UTI Drug Trade Names are Too Similar

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A court case over the trade names of two urinary tract infection (UTI) drugs has been settled. The court ordered that Cipla Medpro be restrained from using the trade name Furizome as it is too similar to Adcock Ingram’s UTI drug Urizone, leading to potential confusion by consumers. In his ruling, Justice James Lekhuleni of the High Court, Western Cape Division, who stated that despite safeguards against confusion in prescribing, ultimately “doctors are human”, so miscommunications could occur – and that the agency of patients cannot be ignored.

The trademark infringement case was brought by three applicants: Adcock Ingram Limited, Adcock Ingram Healthcare (Pty) LTD, and Italian company Zambon S.P.A. Zambon is the owner of the name Urizone, which is used under licence. Urizone had been launched in South Africa in 1993. The applicants stated that more than 3 million sachets had been sold between 2011 and 2023, with R5 million in advertising spent to promote the drug between 2018 and 2022 alone.

The applicants brought the case that Cipla Medpro’s Furizome, with the active ingredient fosfomycin, was too similar to their own product, Urizone, which contained the same ingredient in 3g sachets, and thus could confuse consumers. They alleged that Cipla Medpro sought to capitalise on the reputation earned by Urizone.

The applicants made the case that, despite Urizone being made available as a generic, none of the pharmaceutical companies producing it chose to use the name. When Furizome was launched, Adcock Ingram sent a letter of demand to Cipla to stop using the name due to its . Cipla, through its attorneys, rebutted the claim, saying that the two are sufficiently distinct to avoid confusion, with the “F” alluding to the fosfomycin ingredient. Cipla contended that it had already submitted the name through SAHPRA, and

Cipla also contended that the consumer – the patient – would not be misled during the prescribing and purchase of a schedule 4 medication as they would be informed by the pharmacist of the two different drugs.

In considering the judgment, the court noted that a test as to whether trademarks are be similar can be mode on a phonetic basis, or if they conceptually or visually similar. A trademark’s essential function is to indicate the origin of the goods in connection with which it is used. The “N” and “M” where seen as visually and phonetically similar, and “furi” was similar phonetically to “uri“. This could cause confusion and miscommunication even between doctors as to what drug they had prescribed a patient.

While Justice Lekhuleni acknowledged the safeguards of prescribing schedule 4 medications, he pointed out that the general public had become much more knowledgeable about prescription drugs in the past two decades. On this, he wrote “…the reality is that patients are involved in the process of deciding which medicines they will use, and that creates the risk of confusion. This situation in turn creates a responsibility upon pharmaceutical companies to make sure that they adopt trade marks that are not confusingly similar.”

Leakiness of First Blood–brain Barrier Layer Results in Cognitive Deficits

a, Diagram of the BBB and brain endothelial glycocalyx layer. b, TEM of cortical capillaries with lanthanum nitrate staining from young (3-month-old) and aged (21-month-old) mice. Scale bars, 1 µm. Source: Shi et al., Nature, 2025.

A study published in Nature reveals how a key component of the blood–brain barrier (BBB), the endothelial glycocalyx layer, becomes dysregulated in ageing, causing the BBB to become compromised. The researchers also investigated the possibility of to restore this layer’s integrity, reducing neuroinflammation and restoring cognitive function.

The BBB is a highly specialised safeguard keeping the brain separate from harmful factors, such as toxins and also albumin, IgG and fibrinogen (and, unfortunately, many medications which could otherwise treat brain disease). The leakage of such blood-derived molecules into the brain has been shown to trigger neuroinflammatory changes and create a neurotoxic brain environment. The part of the BBB directly in contact with the blood is the endothelial glycocalyx layer, a carbohydrate-rich meshwork mostly composed of proteoglycans, glycoproteins and glycolipids that coats the BBB lumen. Yet the endothelial glycocalyx’s composition and role is poorly understood despite it being the first layer of interface between the blood and brain.

The researchers found that the brain endothelial glycocalyx is highly dysregulated during ageing and neurodegenerative disease. Two mucin-type O-glycan biosynthetic enzymes, C1GALT1 and B3GNT3 were also found to be downregulated mouse models of ageing and in the brains of Alzheimer’s and Huntington’s disease patients. To test these, the researchers used adeno-associated viruses (AAV) in young mice to turn down the expression of C1GALT1 and B3GNT3. These mice showed signs of BBB leakage and in severe cases, brain haemorrhaging occurred in mice.

In samples from the brains of Alzheimer’s patients, the researchers also observed reduced C1GALT1 in microvessels.

To test if it was possible to restore the BBB’s ability to protect the brain against harmful blood-borne molecules, they administered AAVs in aged mice to restore levels of B3GNT3 and C1GALT1.

Assessing cognitive function, they found that aged mice treated with B3GNT3 via an AAV displayed improvements in spatial working memory in a maze test and hippocampal-dependent learning and memory in a fear conditioning test. Aged mice treated with C1GALT1 did not improve in the maze test, and no significant difference was observed in cued freezing in the fear conditioning among the three aged groups.

Although the study shows that increasing C1GALT1 and B3GNT3 reduces BBB permeability and improves brain health, the precise mechanisms that underlie these beneficial effects remain unclear. The researchers believe that by limiting the nonspecific uptake of blood-derived molecules, the brain can be protected. But C1GALT1 and B3GNT3 are also likely to influence a wide range of proteins and glycan structures and in order to further understand brain ageing and rejuvenation it is therefore crucial to understand the molecular pathways affected by them.

The authors concluded: “Cumulatively, our findings provide a detailed compositional and structural mapping of the ageing brain endothelial glycocalyx layer and reveal important consequences of ageing- and disease-associated glycocalyx dysregulation on BBB integrity and brain health.”

Healthcare Organisations React to US Withdrawal from the WHO

One of the first acts President Trump took on assuming office again on January 20, 2025, was to unilaterally withdraw the United States from the World Health Organization (WHO). Trump complained of the WHO’s “mishandling” of the COVID pandemic, influence by other countries, and the US financial support was excessive compared to China, which “has 300 percent of the population of the United States, yet contributes nearly 90 percent less to the WHO.”

The WHO released a statement, expressing its regret at the decision and pointing out its importance: “WHO plays a crucial role in protecting the health and security of the world’s people, including Americans, by addressing the root causes of disease, building stronger health systems, and detecting, preventing and responding to health emergencies, including disease outbreaks, often in dangerous places where others cannot go.”

The organisation also took aim at Trump’s criticism of its lack of reforms: “With the participation of the United States and other Member States, WHO has over the past 7 years implemented the largest set of reforms in its history, to transform our accountability, cost-effectiveness, and impact in countries. This work continues.”

Critics say that the move would only hand China the opportunity to effectively take control of global health if it chooses to becomes the WHO’s main contributor: though the US is the single largest contributor, it contributed only $1.3 billion in the 2022-23 biennium. An affordable amount compared to the vast sums both countries spend on their militaries. While the WHO did lavish praise on China, many experts saw it as undue and perhaps concerning – but China’s contribution, while currently small, is rising: $86 million in the 2018-19 biennium. After the US, the next largest contributors are Germany ($856 million) and the Bill and Melinda Gates Foundation ($830 million).

The Society for Healthcare Epidemiology of America (SHEA) stressed the importance of global health cooperation. In a statement, the organisation wrote: “It is essential that the United States continues our connection with the WHO to coordinate surveillance, monitoring, detection, prevention, research, and response to public health threats including outbreaks, antimicrobial resistance and high consequence pathogens such as viral haemorrhagic fevers (Ebola, Marburg), Mpox, and highly pathogenic avian influenza (eg, H5N1).”

Indeed, Trump may not simply be able to withdraw by presidential decree; since the US joined the WHO by an act of Congress, it would likely take congressional approval to leave it and Trump may face a lawsuit over this.

Trump previously announced his intention to withdraw the US from the WHO in 2020, something which Gostin et al. warned in The Lancet would not work out well for the US and the world. “Withdrawal from WHO would have dire consequences for US security, diplomacy, and influence. WHO has unmatched global reach and legitimacy.” Additionally, they warned of the sheer difficulty of such a messy divorce: “The US administration would be hard pressed to disentangle the country from WHO governance and programmes.”

Deep Depletion of Blood Lipoprotein(a) Levels with New Drug

Image by Scientific Animations, CC4.0

In a new study, researchers found that a new drug under development, zerlasiran, depleted levels of lipoprotein(a) by more than 80% in participants with increased cardiovascular risk. The drug was well tolerated and the findings, published in JAMA Network, suggest that this could be the first viable treatment for elevated levels of lipoprotein(a).

Elevated levels of lipoprotein(a) (LPa) – a type of cholesterol – is a genetic risk factor for cardiovascular disease. Present in 20% of the population, it increases the risk of atherosclerotic cardiovascular disease (ASCVD) and aortic stenosis. Currently, there are no interventions which can bring down high LPa levels: it is unresponsive to diet, exercise, and other lifestyle changes and there is no available drug.

Zerlasiran, a small-interfering RNA that targets synthesis of LPa serum concentration, was developed to fill this gap. It is effectively a gene silencer that shuts down LPA, a gene which produces a protein found only in LPa. This in turn is expected to reduce cardiovascular risk.

A phase I clinical trial had shown that zerlasiran was safe and effective.

For the study, researchers enrolled 178 patients (average age 63.7 years, 46 female) with ASCVD and LPa concentrations greater than or equal to 125nmol/L. They were randomised to subcutaneously receive zerlasiran 300mg or 450mg, or a placebo, every 16 or every 24 weeks. The least-squares mean placebo-adjusted time-averaged percent change in LPa serum concentrations was −85.6%, −82.8%, and −81.3% for the 450mg every 24 weeks, 300mg every 16 weeks, and 300 mg every 24 weeks groups, respectively. The most common adverse events were injection site reactions, with mild pain occurring in 2.3% to 7.1% of participants in the first day following drug administration. There were 20 serious adverse events in 17 patients, none considered related to the study drug. For the group receiving a 300mcg dose every 16 weeks, it was found that even at the 60 week follow-up, 28 weeks after the last administration, that lipoprotein(a) serum concentrations were still 60% lower than baseline.

New Research Shows that Recombinant Shingles Vaccine Protects Against Dementia

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New research published in Nature has shown that the recombinant shingles vaccine, as with the live version, might have a protective effect against dementia.

While evidence is emerging that the live herpes zoster (shingles) vaccine might protect against dementia, it has now been replaced by recombinant vaccines in many countries. But a lack of data meant that whether the recombinant vaccines conferred the same benefit was unknown. Fortunately, since there was a rapid switch from live to recombinant vaccines, there was an opportunity for a natural experiment to compare the risk of dementia between vaccine types.

The study demonstrated that the recombinant vaccine is associated with a significantly lower risk of dementia in the 6 years post-vaccination. Specifically, receiving the recombinant vaccine is associated with a 17% increase in diagnosis-free time, translating into 164 additional days lived without a diagnosis of dementia in those subsequently affected.

The recombinant shingles vaccine was also associated with lower risks of dementia than were two other vaccines commonly used in older people: influenza and tetanus–diphtheria–pertussis vaccines. The effect was robust across multiple secondary analyses, and was present in both men and women but was greater in women. These findings should stimulate studies investigating the mechanisms underpinning the protection and could facilitate the design of a large-scale randomised control trial to confirm the possible additional benefit of the recombinant shingles vaccine.

Metformin Found to Slow Ageing in Primate Trial

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An exhaustive four year-long study has shown that metformin reduces the effect of ageing. Using a wide array of ageing indicators, the researchers found that metformin resulted in about six year regression in brain ageing. They reported their findings in Cell.

Prior research and anectodal evidence suggested that metformin had an anti-ageing effect. Given to flies, worms and rodents, the drug showed evidence of rejuvenation. People taking metformin also reported feeling younger the longer they took it for.

In a rigorous 40-month study, the researchers gave metformin to 12 elderly male cynomolgus macaques and 18 other cynomolgus monkeys the drug daily. They were aged 13–16 years, equivalent to 40–50 in human years. A control group was used, as well as middle-aged and younger controls to account for ageing effects.

The study encompassed a comprehensive suite of physiological, imaging, histological, and molecular evaluations, substantiating metformin’s influence on delaying age-related phenotypes at the organismal level.

Tissue samples were taken at regular intervals, we leveraged pan-tissue transcriptomics, DNA methylomics, plasma proteomics, and metabolomics to develop innovative monkey aging clocks and applied these to gauge metformin’s effects on ageing.

The results highlighted a significant slowing of aging indicators. A number of organs that seemed to benefit included the kidneys, lungs and the skin. The greatest effect was seen in the brain, however. Metformin exerts a substantial neuroprotective effect, preserving brain structure and enhancing cognitive ability. In this case, treated monkeys had brain activity comparable to those six years younger.

The geroprotective effects on primate neurons were partially mediated by the activation of Nrf2, a transcription factor with anti-oxidative capabilities. The researchers say that this work pioneers the systemic reduction of multi-dimensional biological age in primates through metformin, paving the way for advancing pharmaceutical strategies against human aging.

The researchers have also started a much larger phase 2 human trial, with 120 participants.

One Year On, Eye Transplant Yields Insights to Restoring Vision

The world’s first partial face and whole eye transplant has yielded important insights towards the development of functional eye transplants.

Over one year ago, a surgical team at NYU Langone Health transplanted part of a donor face onto a 46-year old power line worker who had suffered extensive facial injuries and the loss of his left eye. They also transplanted a complete eye into the patient, connecting it up to blood vessels and nerves, to see whether it was possible for an eye to survive. Now, findings on the health of the transplanted eye published in JAMA reveal that the eye is healthy but no light has been seen from it.

For the roughly 40 million people around the world without sight in either eye, stem cell research has been the most recent hope for regaining vision in many cases of trauma and disease.

In the eye transplant, the optic nerve was attached and immunosuppression used. Fluorescein angiography showed that perfusion of the globe and retinal were maintained throughout the immediate postoperative period. Optical coherence tomography revealed atrophy of inner retinal layers and attenuation and disruption of the ellipsoid zone.

Crucially, the retina of the transplanted eye responded to light as confirmed by serial electroretinography. MRI scans demonstrated the integrity of the transplanted visual pathways and potential occipital cortical response to light stimulation of the transplanted eye. However, after one year, no light in the eye was observed by the patient.

As discussed in an accompanying editorial published in JAMA Network, whole eye transplantation (WET) has been regarded as one of the most difficult yet important transplant procedures to attempt developing. In 1978, a report from the National Eye Institute advisory stated that “[a]t present, any effort to transplant a mammalian eye is doomed to failure by the ganglion cell axon’s inability to withstand cutting, by the difficulty of insuring adequate circulation of blood to the transplanted eye during or shortly after operation, and lastly by immune rejection of foreign tissue.”

With this transplant case, the issues of adequate circulation and immune rejection have now been shown to be surmountable, the authors point out. Other issues to address concern connecting the cranial nerves to enable opening of the eyelid.

Engineered T Cells aid the Recovery of Spinal Cord Injury

View of the spinal cord. Credit: Scientific Animations CC4.0

In a recent study published in Nature, researchers prevented T cells from causing the normal autoimmune damage that comes with spinal cord injury, sparing neurons and successfully aiding recovery in mouse models.

In spinal cord injury, the wound site attracts a whole host of peripheral immune cells, including T cells, which result in both beneficial and deleterious effects. Notably, antigen-presenting cells activate CD4+ T cells to release cytokines, ultimately leading to neuroinflammation and tissue destruction. This neuroinflammation is notably most pronounced during the acute phase of spinal cord injury. The problem is that these same T cells have a neuroprotective effect initially, only later developing autoimmunity and attacking the injury site.

Using single cell RNA sequencing, the researchers found that CD4+ T cell clones in mice showed antigen specificity towards self-peptides of myelin and neuronal proteins. Self-peptides have been implicated in a wide range of autoimmune conditions.

Using mRNA techniques, the researchers edited the T cell receptor, so that they shut off after a few days. In mouse models of spinal cord injury, they showed notable neuroprotective efficacy, partly as a result of modulating myeloid cells via interferon-γ.

Their findings provided insights into the mechanisms behind the neuroprotective function of injury-responsive T cells. This will help pave the way for the future development of T cell therapies for central nervous system injuries, and perhaps treatments for neurodegenerative diseases such as Alzheimer’s.